ABSTRACT
A large number of cyclic nucleotide phosphodiesterases have been identified in cardiac muscle. Phosphodiesterase 5 (PDE5) inhibitors reduce cyclic guanosine monophosphate (cGMP) hydrolysis and raise intracellular cGMP content in cardiac and vascular smooth muscle. The consequent pulmonary and systemic vasodilation induced by these drugs may be useful in the treatment of heart failure. The term heart failure has been used in reference to several patterns of cardiac pathophysiology. The level of PDE5 in heart muscle varies from species to species, and may be influenced by the presence of heart disease. The effects of cGMP and protein kinase G in cardiac muscle are less well understood, and appear to be quite complex. The effects of PDE5 inhibition are synergistic with those of inhaled Nitric oxide, which stimulates cGMP formation. The syndrome of greatest importance with respect to the use of PDE3 inhibitors is dilated cardiomyopathy, which, as its name suggests, is characterized by chamber dilatation and impaired cardiac contraction.
